ArticleProceedings of the National Academy of Sciences of the United States of America2013
Beneficial innate signaling interference for antibacterial responses by a Toll-like receptor-mediated enhancement of the MKP-IRF3 axis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Machine learning-driven discovery of host genetic factors for paratuberculosis in goats within the one health framework.BMC veterinary research · 2026Article
- Interferon Regulatory Factor 3 as a Mediator and Therapeutic Target in Innate Immune-Driven Corneal Stromal Inflammation and Opacity.Investigative ophthalmology & visual science · 2026Article
- IRF3 inhibits inflammatory signaling pathways in macrophages to prevent viral pathogenesis.Science advances · 2024Article
- DUSP4 modulates RIG-I- and STING-mediated IRF3-type I IFN response.Cell death and differentiation · 2024Article
- Dual-Specificity Phosphatases in Immunity and Infection: An Update.International journal of molecular sciences · 2019Review
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- Novel chemical compound SINCRO with dual function in STING-type I interferon and tumor cell death pathways.Cancer science · 2018Article
- Stimulator of Interferon Genes Promotes Host Resistance AgainstFrontiers in immunology · 2018Article
- Early IFN type I response: Learning from microbial evasion strategies.Seminars in immunology · 2015Review
- Recognition of tumor cells by Dectin-1 orchestrates innate immune cells for anti-tumor responses.eLife · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 11 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major function of innate immune receptors is to recognize pathogen-associated molecular patterns and then evoke immune responses appropriate to the nature of the invading pathogen(s). Because innate immune cells express various types of these receptors, distinct combinations of signaling pathways are activated in response to a given pathogen. Although the conventional wisdom is that these signaling pathways cooperate with one another to ensure an effective host response, a more nuanced view recognizes antagonism between the individual pathways, where the attenuation of a signaling pathway(s) by others may shape the immune response. In this study, we show that, on Listeria monocytogenes infection, Toll-like receptor-triggered MyD88 signaling pathways suppress type I IFN gene induction, which is detrimental to macrophage bactericidal activity. These pathways target and suppress the IFN regulatory factor 3 (IRF3) transcription factor that is activated by the stimulator of IFN genes-TANK-binding kinase-1 kinase pathway. We also provide evidence for the involvement of the MAPK phosphatase family members, which renders IRF3 hypophosphorylated on Toll-like receptor signaling by enhancing the formation of an MAPK phosphatase-IRF3-TANK-binding kinase-1 ternary complex. This study, therefore, reveals a hitherto unrecognized and important contribution of a beneficial innate signaling interference against bacterial infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.